The invention relates to methods for treating mammals having excess gamma amino butyric acid (GABA) in the central nervous system (CNS). The invention is especially aimed at mammals having visual field defects as a result of excess GABA.
Certain drugs are known to increase GABA levels in the brain (i.e. GABAergic drugs). These drugs are well known to be effective in the treatment of conditions such as seizure disorders.
Recently, it has been discovered that some GABAergic drugs, for example, gamma vinyl GABA (GVG), are also effective for treating and preventing drug addiction. See U.S. Pat. Nos. 6,057,368 and 6,395,783 to Dewey et al., and pending U.S. patent application Ser. Nos. 09/189,166, 09/209,952, 09/362,592, and 09/853,548.
However, there are undesirable side effects, including visual disturbances, associated with the use of GABAergic drugs. In particular, there have been reports of visual field defects (VFDs) associated with the use of GVG. Although the mechanism responsible for GVG-induced VFDs is unknown, it is believed that GVG""s visual toxicity may be related to a significant elevation of GABA levels within the retina. See Comaish, IF et al., xe2x80x9cThe effects of vigabatrin on electrophysiology and visual fields in epileptics: a controlled study with a discussion of possible mechanisms.xe2x80x9d Doc Opthalmol 104:195-212(2002);
It is known that GVG irreversibly inhibits the GABA-degrading enzyme GABA transaminase (GABA-T) and thereby induces an increase in brain GABA levels. It has also been shown that GVG-induced increases in GABA cause a decrease in glutamate decarboxylase (GAD), which is another GABA synthesizing enzyme.
To date, there have been no proposed strategies for treating or preventing the VFDs associated with the use of GABAegic drugs such as GVG. Therefore, there exists a need for a treatment for VFDs associated with the use of GABAergic drugs, such as GVG.
It is thus an object of the present invention to provide a composition and method for treating and/or preventing VFDs associated with the use of GABAergic drugs such as GVG.
The invention provides a method for treating visual field defects in a mammal in need thereof. The method includes administering an effective amount of vitamin B6 to the mammal.
According to the invention, the mammal is preferably a human. The vitamin B6 is administered in an amount from approximately 5 to 300 mg/day, preferably approximately 50 to 100 mg/day and more preferably approximately 10 to 50 mg/day.
In one embodiment of the invention, the mammal is being treated with gamma vinyl GABA for a drug addiction. In another embodiment, the mammal is being treated with gamma vinyl GABA for a seizure disorder.
In accordance with the invention, the vitamin B6 is administered before, simultaneously, or after administration of a GABAergic drug.
The invention also provides novel compositions which include a GABAergic drug and vitamin B6, preferably in a pharmaceutically acceptable carrier. In a preferred embodiment, the GABAergic drug is gamma vinyl GABA.
As a result of the present invention, a method is provided for treating visual field defects associated with excess GABA levels in the central nervous system of a mammal.